1. Central and local regulation of forearm subcutaneous vascular resistance (FSVR) during postural changes were studied in congestive heart failure (CHF). Blood flow was measured by the local 133Xe-washout technique. Nine patients with severe CHF (baseline angiographic ejection fraction, 23 ± 2%, mean ± sem; cardiac index, 2.2 ± 0.2 litres min−1 m−2; increased left ventricular pressures and dimensions) were compared with seven control subjects who had normal cardiac performance.
2. Baseline FSVR and plasma concentrations of noradrenaline and adrenaline were substantially higher in patients with CHF than control subjects. However, the patients, like control subjects, increased FSVR by 46 ± 3% in response to increase in local venous transmural pressure and disclosed a normal response to decrease in forearm perfusion pressure. Both responses to changes in vascular transmural pressure were preserved after either proximal nervous blockade or local β-receptor blockade.
3. Central sympathetic stimulation was induced with use of 45° upright tilt. Control subjects developed vasoconstriction (FSVR increased by 59 ± 5%), which was completely abolished after proximal nerve blockade. Patients with CHF developed vasodilatation (FSVR decreased by 24 ± 8%), which was not only abolished but reversed after proximal nerve blockade (FSVR increased by 22 ± 7%), probably owing to the increased humoral vasoconstrictor activity. The paradoxical vasodilator response to central sympathetic stimulation in these patients was reversed after local β-receptor blockade (FSVR increased by 19 ± 9%).
4. The local vasoconstrictor reflex responsiveness and intrinsic vascular reactivity were not affected by the augmented baseline sympathetic vasoconstrictor activity in patients with CHF. Central sympathetic stimulation seems to elicit a β-adrenergic reflex effect intended to improve perfusion of the subcutaneous tissue in these patients.